HTN

The causes of secondary hypertension include:

- nephrogenic hypertension (mainly parenchymal or renal artery due to renal artery stenosis)
- hormonal disorders (hyperthyroidism and hypothyroidism, primary hyperaldosteronism, Cushing's syndrome, acromegaly,
carcinoid syndrome, pheochromocytoma)
- coarctation of the aorta
- preeclampsia and eclampsia
- severe stress
- obstructive sleep apnea
- increased volume of intravascular fluid
- neurological disorders
– drugs and toxic substances
–
Given a case of Hep C... pt was level f3
According to the recommendations of the Polish Group of HCV Experts and according to the Therapeutic Programs, all patients
infected with HCV should be included in the treatment. Priority in priority is given to patients with advanced fibrosis (> F2 on the
METAVIR scale, F3 means advanced fibrosis, F4 - cirrhosis of the liver). At present, the drugs with the highest efficacy
recommended for treatment are DAA (direct acting antivirals), effective in over 90% of patients. In the DAA era, interferons lost
their importance. In particular, in patients with a history of severe cardiac disease, including unstable or non-treatable cardiac
disease, the use of interferons is contraindicated.
http://www.ghrnet.org/index.php/joghr/article/viewFile/334/357/1391

electrolyte
In patients with chronic carbon dioxide retention compensatory mechanisms are activated - higher levels of carbon dioxide are
tolerated, and there is no decrease in pH due to the increase of bicarbonate levels.
Our patient must have hypercapnication, so as in points A, B, C, without the characteristics of acute acidosis - this is shown in
point B. Point C shows us with completely balanced respiratory acidosis (normal pH, carbon dioxide retention, elevated level
bicarbonate) - it may be a patient with chronic respiratory disease during the period of stabilization between exacerbations. In
point A, we have a lowering of pH (metabolic non-compensated metabolic acid despite the bicarbonate façade) and desaturation
indicating destabilization of the patient.
It should be remembered that the gasometric examination should be assessed together with the clinical condition of the patient -
this is decisive.

Blood

APTT and PT, both are prolonged, why could this be?

At the same time, prolonged kaolin-kephalin (APTT) and prothrombin time (PT) points to damage to two parts of the coagulation
cascade (extrinsic and intrinsic), because prolongation of APTT indicates damage to the intrinsic part and PT to damage to the
extrinsic part.

These causes can be:

A. Congenital eg, deficiency of prothrombin, fibrinogen, factor V or X or deficiencies
B. Acquired e.g. in liver disease, DIC, with supratheraunic doses of anticoagulants, after simultaneous administration of heparin
and oral anticoagulant, administration of a direct thrombin inhibitor, anti-Xa factor or fondaparinux.

TUBERCULOSIS: only use GCS if theres adrenal insufficiency, acute pericarditis, meningitis ...etc

In the case of tuberculosis, the only absolute indication for the use of glucocorticoids (GKS) is adrenal insufficiency as a result of
adrenalectomy by tuberculosis. In addition, GKS are used in:
- acute pericarditis
- meningitis and encephalitis in patients with impaired consciousness and symptoms of increased intracranial pressure
- exudative pleurisy and peritonitis with severe course
- narrowing of airways threatening life
- tuberculosis of lymph nodes with symptoms of pressure on neighboring structures
- severe hypersensitivity reactions to anti-mycobacterial drugs in the absence of substitution with other drugs
- in the inflammatory syndrome in the course of recovery of a normal immune response

LYNCH is not associated with FAP

Lynch syndrome (formerly referred to as HNPCC - hereditary non-polyptic colorectal cancer) is inherited in an autosomal dominant manner; the
mutation of one of the mismatch repair (MMR) genes corresponds to the development of the syndrome. A characteristic feature of this disorder is the
occurrence of many malignant tumors (mainly colon cancer and endometrial cancer) in young people.It is estimated that Lynch's team is responsible
for 1-3% of all cases of colorectal cancer (the most common cause among genetically determined causes). It is NOT associated with polyps
(especially with familial polyposis syndrome). For the most part (approximately 70%) of the cases, the cancer occurs in the right half of the colon. In
the Lynch II syndrome co-occurring tumors of other organs (reproductive system, gastrointestinal tract).
The diagnosis uses the so-called Amsterdam II criteria (all three criteria must be met):
1. three or more relatives with histologically confirmed colorectal cancer, including one first degree relative to the other
2. colorectal carcinoma occurring at least in two generations
3. one or more cases of colon cancer in the family, diagnosed before the age of 50

The most common factors of urinary tract infection are:

in uncomplicated and recurrent inflammation of the bladder:

- E. coli (70-95% of cases)
- Staphylococcus saprophyticus (5-10%)

in uncomplicated acute pyelonephritis:

- E.coli (> 70 to 99%)

in complicated urinary tract infection:

- E.coli (<50%)
- Enterococcus spp (up to 20%)
- Klebsiella (10-15%)
- Pseudomonas (about 10%)

in asymptomatic bacteriuria:
- in women - E. coli
- in patients with a long-term catheter - several microorganisms, among them Pseudomonas spp. and Proteus spp.

Up to 30% of infections are caused by Chlamydia, gonorrhea and viruses, and about 5% of complicated infections cause fungi.

WHAT PREDISPOSES to HYPERCALCEMIA:

Hypothyroidism leads to hypocalcaemia.

The reasons for HIPERkalcemia include

- tumors,
- primary hyperparathyroidism,
- sarcoidosis,
- multiple myeloma,
- vitamin D poisoning,
- vitamin A poisoning (increased osteolysis),
- lithium (side effects of lithium may be: hypothyroidism, hyperparathyroidism),
- thiazide diuretics - reduce they are calciuria and can be used to treat hypocalcaemia as a complementary treatment.
- overactive thyroid gland (increased osteolysis), - milk-alkaline syndrome (excessive use of calcium carbonate, calcium-containing
gastric antacids or excessive consumption of dairy products)
- long-term immobilization

REASONS FOR HYPER AND HYOP CALCEMIA:

The reasons for HIPERkalcemia include
- tumors,
- primary hyperparathyroidism,
- sarcoidosis,
- multiple myeloma,
- vitamin D poisoning,
- vitamin A poisoning (increased osteolysis),
- lithium (side effects of lithium may be: hypothyroidism, hyperparathyroidism),
- thiazide diuretics - reduce they are calciuria and can be used to treat hypocalcaemia as a complementary treatment.
- hyperthyroidism (increased osteolysis),
- long-term immobilization
- milk-alkaline syndrome (excessive use of calcium carbonate, calcium-containing gastric antacids or excessive consumption of
dairy products).

The causes of HIPOcalcuria include:

- too low supply of calcium with food
- impaired absorption from the gastrointestinal tract (vitamin D deficiency, malabsorption syndromes)
- too much calcium deposition in soft tissues / bones (OZT, bones hungry syndrome, bisphosphonates)
- too much loss of calcium in the urine (diuretics loop, tubular acidosis)
- parathromon deficiency (hypoparathyroidism)
- hyperphosphatemia
- tumor decay syndrome
- calcimimetics are drugs used to treat secondary hyperparathyroidism, reduce PTH, may cause hypocalcaemia.

MGMT of Acute Pulmonary Embolism:

In the acute phase of pulmonary embolism:

- in high-risk patients
– fibrinolytics (eg recombinant plasminogen activator), unfractionated heparin followed by oral anticoagulants (vitamin K
antagonists, Xa factor inhibitors, direct thrombin inhibitors)
- in low-risk patients
– - low-molecular-weight heparin, fondaparinux and then oral anticoagulants (vitamin K antagonists, factor Xa inhibitors,
direct thrombin inhibitors)

. Antiplatelet drugs are not used.

THROMBOEMBOLIC RISK- CHADS-VASC

According to the recommendations of the European Cardiac Society / Polish Cardiac Society for thromboembolic prophylaxis in
patients with atrial fibrillation / flutter and CHADS-VASc = 1 score, anticoagulation should be considered, and in patients with a
score of 2 and more it is recommended. It is not used in the prophylaxis of antiplatelet treatment, unless, as a last resort, if the
patient can not take anticoagulant therapy (vitamin K antagonists or new oral thrombotic drugs).
Prevention is not required for people with a score of 0 or women up to 65 years of age, where gender is the only risk factor.

The CHA2DS2-VASc scale is an acronym, and the score in it is as follows:

C - heart failure - 1 point.
H - arterial hypertension - 1 point
A - age> = 75 years - 2 points
D - diabetes - 1 point
S - stroke or TIA - 2 points
V - vascular disease - 1 point
A - age 65-74 - 1 point
Sc - female sex - 1 point

Our patient has 1 point for sex, age, hypertension and diabetes, a total of 4 points and requires anticoagulative therapy.

CARDIAC TAMPONADE sx
Possible symptoms of cardiac tamponade are:
- tachycardia
- bizarre (paradoxical) heart rate, i.e. a decrease in systolic BP> 10 mmHg on the inhale
- widening of the jugular veins (due to increased central venous pressure)
- reduction of heart tones (sound isolation of the heart by the presence of fluid)
- small amplitude of waves on the ECG (electrical insulation of the heart by the presence of fluid)
- hypotension

Historically, Beck's triad stood out: hypotonia, silent heart tones, excessively filled cervical veins

ANTIDOTES:

Acetaminophen -> N-acetylcysteine

Glucagon -> beta-blockers (along with atropine)

naloxone -> opioid poisoning

deferoxamine ->iron poisoning.

organophosphorus agents (symptoms of cholinergic syndrome) is pralidoxime and other drugs from the group of
acetylcholinesterase reactors (oximes). Also atropine may be used in poisoning with organophosphorus.